TNF decreases food intake and body weight gain in rats, but with repeated i.p. administration rats become tolerant to the effects of TNF on food intake and body weight gain.1 When tolerant rats are given a subsequent inoculation of sarcoma, they live significantly longer than control non-tolerant rats.1 Rats tolerant to TNF's effects on food intake and body weight are also tolerant to a lethal injection of TNF or endotoxin (LPS).2 Tolerance to LPS also protects against TNF.2 However, the mechanisms of tolerance to LPS and TNF are not the same, because LPS tolerance decreases macrophage secretion of TNF and TNF tolerance increases macrophage secretion of TNF.3 Sarcoma-bearing rats have circulating cachectin activity in their serum and levels increase as food intake decreases, body weight decreases and tumor burden increases.4 Tumor resection reverses serum cachectin activity levels.4 This experiment4 plus the previous one1 suggest that TNF is a mediator of cachexia in this rat model. This sarcoma has high-affinity glucocorticoid receptors which regulate its growth.5 Insulin is able to reverse the toxic effects of TNF including effects on body weight, food intake and histology.6 Insulin is also able to improve the body composition of sarcoma-bearing rats preserving lean body and fat mass,7 and in some experiments insulin can improve the survival of cachectin TB rats.8 Gastrinomas in patients with ZES can be occult and difficult to find at surgery. We prospectively compared operative ultrasound to palpation to localize gastrinomas and found that each procedure complements each other.9 In addition, we demonstrated more effective management of gastric acid hypersecretion by parathyroidectomy in patients with ZES, hyperparathyroidism and MEN-I.10 Finally, we demonstrated a 40% objective response rate of combination chemotherapy including streptozotocin, 5 FU and doxorubicin in patients with metastatic gastrinoma.11